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Titolo:
DRUG-INDUCED IN-VITRO INHIBITION OF NEUTROPHIL-ENDOTHELIAL CELL-ADHESION
Autore:
PELLEGATTA F; LU Y; RADAELLI A; ZOCCHI MR; FERRERO E; CHIERCHIA S; GAJA G; FERRERO ME;
Indirizzi:
UNIV MILAN,IST PATOL GEN,VIA MANGIAGALLI 31 I-20133 MILAN ITALY UNIV MILAN,IST PATOL GEN I-20133 MILAN ITALY UNIV MILAN,CTR STUDIO PATOL CELLULARE I-20133 MILAN ITALY IST SCI SAN RAFFAELE,CARDIOVASC PATHOPHYSIOL LAB MILAN ITALY IST SCI SAN RAFFAELE,LAB ADOPT IMMUNOTHERAPY MILAN ITALY
Titolo Testata:
British Journal of Pharmacology
fascicolo: 3, volume: 118, anno: 1996,
pagine: 471 - 476
SICI:
0007-1188(1996)118:3<471:DIIONC>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; GRAFTED RAT HEARTS; METABOLIC FUNCTION; POSTISCHEMIC REPERFUSION; DEFIBROTIDE TREATMENT; IMMUNE-SYSTEM; PROCUREMENT; ISCHEMIA; INJURY; DAMAGE;
Keywords:
CHEMOATTRACTANT; CYTOKINES; DEFIBROTIDE; INTEGRINS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
40
Recensione:
Indirizzi per estratti:
Citazione:
F. Pellegatta et al., "DRUG-INDUCED IN-VITRO INHIBITION OF NEUTROPHIL-ENDOTHELIAL CELL-ADHESION", British Journal of Pharmacology, 118(3), 1996, pp. 471-476

Abstract

1 Leukocyte-endothelial cell interactions play an important role during ischaemia-reperfusion events. Adhesion molecules are specifically implicated in this interaction process. 2 Since defibrotide has been shown to be an efficient drug in reducing damage due to ischaemia-reperfusion in many experimental models, we analysed the effect of defibrotide in vitro on leukocyte adhesion to endothelial cells in basal conditions and after their stimulation. 3 In basal conditions, defibrotide (1000 mu g ml(-1)) partially inhibited leukocyte adhesion to endothelial cells by 17.3%+/-3.6 (P<0.05), and after endothelial cell stimulation (TNF-alpha, 500 u ml(-1)) or after leukocyte stimulation (fMLP, 10(-7) M), it inhibited leukocyte adhesion by 26.5%+/-3.4 and 32.4%+/-1.8,respectively (P<0.05). 4 In adhesion blockage experiments, the use ofthe monoclonal anntibody anti-CD31 (5 mu g ml(-1)) did not demonstrate a significant inhibitory effect whereas use of the monoclonal antibody anti-LFA-1 (5 mu g ml(-1)) significantly interfered with the effectof defibrotide. 5 This result was confirmed in NIH/3T3-ICAM-1 transfected cells. 6 We conclude that defibrotide is able to interfere with leukocyte adhesion to endothelial cells mainly in activated conditions and that the ICAM-1/LFA-1 adhesion system is involved in the defibrotide mechanism of action.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 13:11:51